Nuclear hormone receptors respond rapidly to their ligands to trigger signaling cascades independent of transcription. More recent discoveries revealed various levels of cross-talk between nongenomic and genomic responses of nuclear receptors with, for example, kinase cascades mobilized by activation of cytoplasmic and/or plasma membrane localized nuclear receptors exerting direct and indirect effects on the transcriptional program regulated by genome-associated receptors. Such crosstalk has even been shown to have an impact on intercellular steroid hormone action and influence organ physiology. Therefore, this is a prime period in the nuclear receptor field to be considering new and innovative approaches to examine system-wide crosstalk between rapid, nongenomic nuclear receptor signaling with classical genome-wide action. The purpose of this conference is to bring together a diverse group of scientists (junior, senior and trainees) with expertise ranging from endocrinology, energy metabolism, neuroendocrinology, epigenetics, environmental endocrine disruptors, cardiovascular function, reproduction, immunology, neurobiology and cancer to present exciting new discoveries that uncover fresh insights into system-wide action of nuclear hormone receptors acting at nongenomic and genomic levels. The diversity of this conference will foster and stimulate innovative ideas through the establishment of new collaborations or experimental approaches generated by exposure to the many model systems and provocative results of the speakers. National and international leaders in the fields of nongenomic or genomic steroid hormone signaling will present their most recent, unpublished work that focuses on intracellular or intercellular integration of these two pathways. Furthermore ample opportunities will be given to trainees and junior investigators to present their work and meet with senior investigators. In summary, this conference will stimulate the development of new therapeutic approaches to tackle complex human diseases that result from dysregulation of a recognized family of druggable targets, the nuclear receptors.